DESCRIPTION (The applicant's description verbatim): Despite improved management strategies for AMI, proper selection of patients for these strategies is still in its infancy. One of the main reasons is the use of insensitive markers of acute coronary occlusion, reperfusion, and infarction in the clinical setting. Routine use of the EKG and cardiac enzymes in patients with AMI, although inexpensive and easy to perform, has limited our ability to select individual patients for customized treatment. For instance, we still use EKG to diagnose AMI despite the fact that only one-third to two-fifth of all AMI patients have a diagnostic EKG at the time of hospital presentation. We use cardiac enzymes for the confirmation of AMI, but these become positive several hours after coronary occlusion, and are of little value in determining immediate management strategies for patients with AMI. The infarct size can be no larger than the risk area (the region with hypoperfusion after a coronary artery is occluded). If the risk area is small, thrombolysis may not be worth the risk and angioplasty may not be worth the cost. If there is adequate collateral MBF within the risk area that will maintain myocardial viability, immediate intervention may not even be necessary. On the other hand, if thrombolysis fails to achieve tissue reperfusion, rescue angioplasty with or without a drug that limits microvascular injury may be indicated. Finally, the transmural extent of infarction may determine which patient will most benefit from an ACE inhibitor. At present, we do not stratify patients in a manner to optimize their treatment. We hypothesize that by imaging the myocardial microvasculature in patients with suspected AMI we can: 1) detect AMI and determine the ultimate infarct size despite persistent coronary occlusion. 2) Determine the success of tissue reperfusion and the effect of intravenous administration of adenosine on coronary microvascular perfusion and infarct size. 3) Determine the effect of the extent of microvascular abnormalities after AMI on LV remodeling and the effect of an ACE inhibitor that causes angiogenesis on this remodeling; and 4) Determine the long-term prognostic value of normal and abnormal microvascular perfusion patterns after the initial management of AMI. We will study the myocardial microvascular using myocardial contrast echocardiography, a newly developed technique that can provide a noninvasive assessment of the myocardial microvasculature in humans. The study aims will be to test the 4 above-mentioned hypotheses in patients with suspected AMI.